Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19, leading to cytotoxic depletion of CD19+ B-lineage cells and a B-cell reset in SLE.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CD19. Upon binding CD19 on B-lineage cells, the CAR T cells become activated and mediate cytotoxic killing of CD19+ B cells and plasmablasts, leading to B-cell depletion and subsequent immune reset with reduced autoantibody production and inflammatory signaling.
YES
DIRECT
CD19-targeted CAR T cells bind CD19 on B-lineage cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
CRISPR-edited, allogeneic, second-generation anti-CD19 CAR-T (FMC63 scFv; CD28 costimulatory and CD3ζ signaling domains) with TRAC knockout to remove endogenous TCR and SPPL3 (Power3) knockout to alter glycosylation (“glycan shielding”), aiming to reduce GVHD, lessen alloimmune recognition, and improve persistence against CD19+ malignant B cells.
CRISPR-edited, allogeneic second-generation anti-CD19 CAR-T cells (FMC63 scFv with CD28 costimulation and CD3ζ signaling) mediate CAR-driven activation and cytotoxic killing of CD19+ B cells. TRAC knockout removes the endogenous TCR to reduce graft-versus-host disease, while SPPL3 (Power3) knockout alters glycosylation to lessen alloimmune recognition and enhance persistence/expansion.
YES
DIRECT
Anti-CD19 CAR-T cells bind CD19 on target B cells, triggering CD28/CD3ζ signaling and formation of an immunologic synapse that mediates perforin/granzyme release (and death-receptor signaling), inducing apoptosis of CD19+ cells.
CRISPR-edited, allogeneic, second-generation anti-CD19 CAR-T (FMC63 scFv; CD28 costimulatory and CD3ζ signaling domains) with TRAC knockout to remove endogenous TCR and SPPL3 (Power3) knockout to alter glycosylation (“glycan shielding”), aiming to reduce GVHD, lessen alloimmune recognition, and improve persistence against CD19+ malignant B cells.
CRISPR-edited, allogeneic second-generation anti-CD19 CAR-T cells (FMC63 scFv with CD28 costimulation and CD3ζ signaling) mediate CAR-driven activation and cytotoxic killing of CD19+ B cells. TRAC knockout removes the endogenous TCR to reduce graft-versus-host disease, while SPPL3 (Power3) knockout alters glycosylation to lessen alloimmune recognition and enhance persistence/expansion.
NO
INDIRECT
These CAR-T cells kill CD19+ B cells via CAR-mediated cytotoxicity (perforin/granzyme apoptosis). TRAC is knocked out in the CAR-T product and is not a recognized target; TRAC-expressing cells are not directly targeted or killed.
CRISPR-edited, allogeneic, second-generation anti-CD19 CAR-T (FMC63 scFv; CD28 costimulatory and CD3ζ signaling domains) with TRAC knockout to remove endogenous TCR and SPPL3 (Power3) knockout to alter glycosylation (“glycan shielding”), aiming to reduce GVHD, lessen alloimmune recognition, and improve persistence against CD19+ malignant B cells.
CRISPR-edited, allogeneic second-generation anti-CD19 CAR-T cells (FMC63 scFv with CD28 costimulation and CD3ζ signaling) mediate CAR-driven activation and cytotoxic killing of CD19+ B cells. TRAC knockout removes the endogenous TCR to reduce graft-versus-host disease, while SPPL3 (Power3) knockout alters glycosylation to lessen alloimmune recognition and enhance persistence/expansion.
NO
INDIRECT
SPPL3 is not targeted by the CAR; the CAR-T cells kill only CD19+ cells via T-cell cytolysis (perforin/granzyme, Fas/FasL). SPPL3 is knocked out in the CAR-T cells to reduce immunogenicity and does not mediate target-cell killing.
Humanized IgG monoclonal antibody (JSP191) administered subcutaneously that targets CD117 (c‑Kit), blocking SCF–c‑Kit signaling to deplete/inhibit KIT+ cells, especially tissue mast cells, thereby reducing mediator release in chronic urticaria.
Humanized IgG monoclonal antibody targeting CD117 (c‑Kit) that blocks stem cell factor (SCF) binding/signaling, leading to depletion or inhibition of KIT+ cells—particularly mast cells and hematopoietic stem/progenitor cells—thereby reducing mast-cell survival/activation and mediator release.
YES
DIRECT
Binds CD117 and blocks SCF–c‑Kit survival signaling, leading to apoptosis/depletion of KIT+ cells (with potential contribution from Fc-mediated effector functions).